ArticleDrug design, development and therapy2025
Integrating Network Pharmacology and Experimental Validation to Investigate the Action Mechanism of Allicin in Atherosclerosis.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Multi-omics and network pharmacology identify IGFBP1 as an m6A-Epigenetic target of pueraria in NSCLC therapy.PLoS computational biology · 2026Article
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Authors and funding
10 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Allicin is a monomer compound derived from traditional Chinese medicine, which has demonstrated significant efficacy in the treatment of cancer, neuroinflammation, gastrointestinal diseases, and other conditions. However, the specific mechanism of action of Allicin in combating cardiovascular diseases remains insufficiently clarified, which limits its application in therapy. Methods: Network pharmacology and molecular docking techniques were employed to explore the potential targets and signaling pathways of Allicin in the treatment of as atherosclerosis (AS). The regulatory effects of Allicin on cell apoptosis, aortic plaques, and lipid levels were assessed through TUNEL staining, Oil Red O staining, HE staining, GPO-PAP, and COD-PAP. Additionally, immunofluorescence assay was conducted to validate the screened key targets. Results: Based on the analysis of network pharmacology and molecular docking techniques, 94 predicted overlapping target genes were identified from the target genes of Allicin and AS-related target genes; Among them, Allicin exhibits a strong binding affinity for five main targets (CASP3, NF-κB1, BTK, MAPK3, and PARP1), and these targets were found to play important role in the anti-apoptotic mechanism of Allicin. Furthermore, Allicin could inhibit the progression of plaques, down- regulating the expressions of CASP3 and NF-κB1, and up-regulate the expressions of BTK, MAPK3, and PARP1 in vivo and in vitro. Conclusion: The present results show that Allicin may improves AS by regulating the main targets of macrophage apoptosis.
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